The contrasting phylodynamics of human influenza B viruses

Vijaykrishna, Dhanasekaran; Holmes, Edward C.; Joseph, Udayan; Fourment, Mathieu; Su, Yvonne C. F.; Halpin, Rebecca; Lee, Raphael Tze Chuen; Deng, Yi‐Mo; Gunalan, Vithiagaran; Lin, Xudong; Stockwell, Timothy B.; Fedorova, Nadia; Zhou, Bin; Spirason, Natalie; Kühnert, Denise; Bošková, Veronika; Stadler, Tanja; Costa, Anna‐Maria; Dwyer, Dominic E.; Huang, Q. Sue; Jennings, Lance C.; Rawlinson, William D.; Sullivan, Sheena G.; Hurt, Aeron C.; Maurer‐Stroh, Sebastian; Wentworth, David E.; Smith, Gavin J. D.; Barr, Ian G.

doi:10.7554/elife.05055

Cited by 205 publications

(268 citation statements)

References 62 publications

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“…Nevertheless, both lineages cocirculated each year. Data from other countries and from another Australian study found that B/Victoria cases were younger than cases with B/Yamagata infection 33, 54, 55. Our results showed the only age group with a trend towards a higher proportion of Victoria lineage was 10‐ to 19‐year‐olds.…”

Section: Discussionsupporting

confidence: 48%

“…Mismatch between the TIV's influenza B lineage and the circulating B lineage occurs at approximately two‐ to four‐year intervals in many countries 18. In Australia, partial or complete mismatches of B with circulating lineage have been reported 33. It is not fully understood whether vaccination with one B lineage confers significant protection against the other.…”

Section: Introductionmentioning

confidence: 99%

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Epidemiology of influenza B in Australia: 2001‐2014 influenza seasons

Moa

Muscatello

Turner

et al. 2016

Influenza Resp Viruses

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BackgroundInfluenza B is characterised by two antigenic lineages: B/Victoria and B/Yamagata. These lineages circulate together with influenza A during influenza seasons, with varying incidence from year to year and by geographic region.ObjectiveTo determine the epidemiology of influenza B relative to influenza A in Australia.MethodsLaboratory‐confirmed influenza notifications between 2001 and 2014 in Australia were obtained from the Australian National Notifiable Diseases Surveillance System.ResultsA total of 278 485 laboratory‐confirmed influenza cases were notified during the study period, comprising influenza A (82.2%), B (17.1%) and ‘other and untyped’ (0.7%). The proportion of notifications that were influenza B was highest in five‐ to nine‐year‐olds (27.5%) and lowest in persons aged 85 years and over (11.5%). Of all B notifications with lineage determined, 77.1% were B/Victoria and 22.9% were B/Yamagata infections. Mismatches between the dominant B lineage in a season and the trivalent vaccine B lineage occurred in over one‐third of seasons during the study years. In general, influenza B notifications peaked later than influenza A notifications.ConclusionThe proportion of circulating influenza B in Australia during 2001‐2014 was slightly lower than the global average and was dominated by B/Victoria. Compared with influenza A, influenza B infection was more common among older children and young adults and less common in the very elderly. Influenza B lineage mismatch with the trivalent vaccine occurred about one‐third of the time.

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Section: Discussionsupporting

confidence: 48%

Section: Introductionmentioning

confidence: 99%

Epidemiology of influenza B in Australia: 2001‐2014 influenza seasons

Moa

Muscatello

Turner

et al. 2016

Influenza Resp Viruses

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“…Influenza A viruses attract the greatest attention due to infrequent infections of humans with zoonotic viruses, the potential to give rise to pandemic viruses through genetic reassortment and antigenic shift, sustained antigenic drift, extensive spread, and varied severities of disease (1). In contrast, influenza B viruses are confined largely to humans, antigenic drift of these viruses occurs at a lower rate, and these viruses do not undergo antigenic shift (1,2). The severity of disease caused by influenza virus is considered unpredictable (3), yet, until recently, infections with influenza B viruses were considered to be mild compared to infections with influenza A viruses (4) and to account for a reduced burden of disease.…”

mentioning

confidence: 99%

Characterization of the Localized Immune Response in the Respiratory Tract of Ferrets following Infection with Influenza A and B Viruses

Carolan

Rockman

Borg

et al. 2016

J Virol

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The burden of infection with seasonal influenza viruses is significant. Each year is typically characterized by the dominance of one (sub)type or lineage of influenza A or B virus, respectively. The incidence of disease varies annually, and while this may be attributed to a particular virus strain or subtype, the impacts of prior immunity, population differences, and variations in clinical assessment are also important. To improve our understanding of the impacts of seasonal influenza viruses, we directly compared clinical symptoms, virus shedding, and expression of cytokines, chemokines, and immune mediators in the upper respiratory tract (URT) of ferrets infected with contemporary A(H1N1)pdm09, A(H3N2), or influenza B virus. Gene expression in the lower respiratory tract (LRT) was also assessed. Clinical symptoms were minimal. Overall cytokine/chemokine profiles in the URT were consistent in pattern and magnitude between animals infected with influenza A and B viruses, and peak expression levels of interleukin-1␣ (IL-1␣), IL-1␤, IL-6, IL-12p40, alpha interferon (IFN-␣), IFN-␤, and tumor necrosis factor alpha (TNF-␣) mRNAs correlated with peak levels of viral shedding. MCP1 and IFN-␥ were expressed after the virus peak. Granzymes A and B and IL-10 reached peak expression as the virus was cleared and seroconversion was detected. Cytokine/chemokine gene expression in the LRT following A(H1N1)pdm09 virus infection reflected the observations seen for the URT but was delayed 2 or 3 days, as was virus replication. These data indicate that disease severities and localized immune responses following infection with seasonal influenza A and B viruses are similar, suggesting that other factors are likely to modulate the incidence and impact of seasonal influenza. IMPORTANCEBoth influenza A and B viruses cocirculate in the human population, and annual influenza seasons are typically dominated by an influenza A virus subtype or an influenza B virus lineage. Surveillance data indicate that the burden of disease is higher in some seasons, yet it is unclear whether this is due to specific virus strains or to other factors, such as cross-reactive immunity or clinical definitions of influenza. We directly compared disease severities and localized inflammatory responses to different seasonal influenza virus strains, including the 2009 pandemic strain, in healthy naive ferrets. We found that the disease severities and the cytokine and chemokine responses were similar irrespective of the seasonal strain or the location of the infection in the respiratory tract. This suggests that factors other than the immune response to a particular virus (sub)type contribute to the variable impact of influenza virus infection in a population. Morbidity and mortality associated with human influenza virus infection are significant worldwide. Influenza is caused by three virus types (A, B, and C), among which types A and B are responsible for most of the diagnosed cases of seasonal influenza. Influenza A viruses attract the greatest attentio...

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“…The Victoria lineage is subject to stronger seasonal bottlenecks, higher transmission rates, greater antigenic variation, and stronger positive selection and infects mostly younger age groups. In contrast, the Yamagata lineage experiences less severe bottlenecks and infects older people (3). In tropical Kuala Lumpur in Malaysia, there is year-round influenza activity, with biannual epidemics in May to July and November to January (4).…”

mentioning

confidence: 99%

Evolution of Influenza B Virus in Kuala Lumpur, Malaysia, between 1995 and 2008

Sam

Chan

et al. 2015

J Virol

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g Influenza B virus causes significant disease but remains understudied in tropical regions. We sequenced 72 influenza B viruses collected in Kuala Lumpur, Malaysia, from 1995 to 2008. The predominant circulating lineage (Victoria or Yamagata) changed every 1 to 3 years, and these shifts were associated with increased incidence of influenza B. We also found poor lineage matches with recommended influenza virus vaccine strains. While most influenza B virus lineages in Malaysia were short-lived, one circulated for 3 to 4 years.

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The contrasting phylodynamics of human influenza B viruses

Cited by 205 publications

References 62 publications

Epidemiology of influenza B in Australia: 2001‐2014 influenza seasons

Epidemiology of influenza B in Australia: 2001‐2014 influenza seasons

Characterization of the Localized Immune Response in the Respiratory Tract of Ferrets following Infection with Influenza A and B Viruses

Evolution of Influenza B Virus in Kuala Lumpur, Malaysia, between 1995 and 2008

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